NEUROTROPHIC ULCERS

                          NEUROTROPHIC ULCERS

Neurotrophic Ulcers

The development of neurotrophic foot ulcers in patients with diabetes mellitus has several components, including neuropathy, biomechanical pressure, and vascular supply. Peripheral neuropathy is clearly the dominant factor in the pathogenesis of diabetic foot ulcers.
The neuropathy associated with diabetes is a distal symmetrical sensorimotor polyneuropathy. There is a clear correlation between the presence of hyperglycemia and the development of neuropathy. The mechanism by which this occurs, although extensively studied, continues to be investigated. Much attention has been focused on the polyol pathway. This pathway may result in the deposition of sorbitol within peripheral nerves. In addition, oxygen radicals may be produced, which may contribute to nerve damage. Vascular disease of nerve-supplying vessels may contribute to neuropathy. More recently, increased susceptibility to compression in diabetic patients as a contributor to the development of neuropathy has been postulated.
The sensory component of the neuropathy results in a decreased ability to perceive pain from foreign bodies, trauma, or areas of increased pressure on the foot. Loss of sensation accompanied by trauma or increased pressure contributes to skin breakdown, often accompanied by ulcer formation at the site of pressure.
The motor component of neuropathy can lead to atrophy of the intrinsic musculature of the foot, resulting in digital contractures and areas of elevated pressure on the plantar foot. In addition, weakness of the anterior leg musculature may contribute to equinus deformity with lack of adequate dorsiflexion at the ankle joint, leading to elevated plantar pressures in the forefoot.
Autonomic neuropathy may occur, with loss of sympathetic tone and arteriovenous shunting of blood in the foot. Sweat glands may also be affected; the resultant anhidrosis leads to dry, cracked skin and predisposes the skin to breakdown.
There is a well-established association between diabetes and increased risks for the development of atherosclerosis and peripheral arterial disease. This is more likely to occur in smokers. This is not microvascular but macrovascular disease, predominantly of the infragenicular (tibial and peroneal arteries) vessels, with sparing of the vessels in the foot. Ischemia may therefore contribute at least in part to the development or persistence of foot ulcers in diabetic patients